High Nutrient Concentration Can Induce Virulence Factor Expression and Cause Higher Virulence in an Environmentally Transmitted Pathogen

Abstract

Environmentally transmitted opportunistic pathogens shuttle between two substantially different environments: outside-host and within-host habitats. These environments differ from each other especially with respect to nutrient availability. Consequently, the pathogens are required to regulate their behavior in response to environmental cues in order to survive, but how nutrients control the virulence in opportunistic pathogens is still poorly understood. In this study we examined how nutrient level in the outside-host environment affects the gene expression of putative virulence factors of the opportunistic fish pathogen Flavobacterium columnare. The impact of environmental nutrient concentration on bacterial virulence was explored by cultivating the bacteria in various nutrient conditions, measuring the gene expression of putative virulence factors with RTqPCR, and finally, experimentally challenging rainbow trout (Oncorhynchus mykiss) fry with these bacteria. Our results show that increased environmental nutrient concentration can increase the expression of putative virulence genes, chondroitinase (cslA) and collagenase, in the outside-host environment and may lead to more rapid fish mortality. These findings address that the environmental nutrients may act as significant triggers of virulence gene expression and therefore contribute to the interaction between an environmentally transmitted opportunistic pathogen and its host.

Higher resource level promotes virulence in an environmentally transmitted bacterial fish pathogen

“…In contrast, while nutrient addition also led to improved bacterial replication compared to the baseline level, the growth between the low‐ and high‐nutrient environments did not differ. This result indicates that in addition to the increased outside‐host growth of the pathogen, increased nutrient availability is likely to promote bacterial virulence via virulence factor activation (Penttinen, Kinnula, Lipponen, Bamford, & Sundberg, ). Taken together, our results suggest that fluctuations in environmental nutrient conditions can have immediate effects on disease dynamics and outbreak severity.…”

Response of host–bacterial colonization in shrimp to developmental stage, environment and disease

“…However, when the gut histology and availability niches change as the host ages, the initial "winners" will be reassembled, thereby resulting in a host stage-specific gut microbiota (Greenhalgh et al, 2016;Stephens et al, 2015;Xiong et al, 2018;Yan et al, 2016). Instead, water quality tends to be deteriorative and eutrophic over shrimp cultivation (Xiong et al, 2014;Yang et al, 2018), which stresses shrimp and increases the virulence of pathogens (Penttinen, Kinnula, Lipponen, Bamford, & Sundberg, 2016). In turn, shrimp relocate energy in response to pathogen invasion, thereby attenuating their filtering abilities.…”

The Western Diet–Microbiome-Host Interaction and Its Role in Metabolic Disease

“…Gut bacteria adjust their metabolism according to both the substances produced by other microbes and the nutrient supply, which may produce effects that influence metabolic and inflammatory pathways in the human body [31]. For instance, both human and animal studies have demonstrated that pathogens, pathobionts and other members of the microbiome can respond to a change in their environment (e.g.the presence of some emulsifiers; discussed later) by increasing expression of virulence factors [32][33][34], thereby increasing the pro-inflammatory potential of the microbiome Major changes in diet and subsequent changes in microbiota can, at least to some extent, be reversed within the same generation. However, recent studies in rodents have demonstrated that loss of microbiota diversity due to dietary changes can be transferred to later generations , with progressive loss of diversity [35].…”

“…It is likely that abundance of accessible nutrients in the small intestine of animals signal large nutrient availability and sufficient resources to expand the bacteria's territory [32,46]. These effects could propagate further down the digestive system.…”